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1 anol (as a model of binge drinking and acute ethanol intoxication).
2 ble opening were affected by both hunger and ethanol intoxication.
3 imethoxybenzyl)piperazine (NP078585) reduced ethanol intoxication.
4 , regulate different manifestations of acute ethanol intoxication.
5 Adenosine is an important mediator of ethanol intoxication.
6 in undrugged performance and sensitivity to ethanol intoxication.
7 ls in both the absence and presence of acute ethanol intoxication.
8 e to endotoxin in rats with or without acute ethanol intoxication.
9 a dose rated as similar to greater levels of ethanol intoxication.
10 he long-term effects of chronic intermittent ethanol intoxication.
11 l inhibitors may be useful in reducing acute ethanol intoxication and alcohol consumption by human al
13 ur understanding of their functional role in ethanol intoxication and consumption is very limited.
17 provide a molecular basis for understanding ethanol intoxication and the likely effects of human pol
22 vation during testing did not substitute for ethanol intoxication, demonstrating that the effects of
26 ethanol and acetaldehyde levels after acute ethanol intoxication in both wild-type and ALDH2-deficie
30 hdrawal (MW) experience (four cycles of 16 h ethanol intoxication interrupted by 8 h periods of absti
31 eriod of synaptogenesis, a single episode of ethanol intoxication lasting for several hours triggers
32 ice with beta-catenin-deficient hepatocytes, ethanol intoxication led to significant redox imbalance
35 examined mice for the effect of either acute ethanol intoxication or Adh1 gene disruption on RA synth
37 affecting ethanol metabolism, sensitivity to ethanol intoxication, or continuous-access drinking.
38 following 16 h (SW) or 64 h (CE) continuous ethanol intoxication, or no ethanol exposure (controls).
43 ic transmission by ethanol may contribute to ethanol intoxication, reinforcement, tolerance, and depe
47 cover neuronal molecular correlates of acute ethanol intoxication, we used stable-isotope-labeled mic